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Severe lung disease in COVID-19 is primarily driven by a hyperactive immune response leading to an infiltration of pro-inflammatory cells and cytokines. A possible explanation for the "cytokine storm" associated with SARS-CoV-2 is the inhibition of the IFN-inducing signaling pathway impacting the ability of the host to block viral replication, as previously observed in SARS-CoV-1 and MERS-CoV infection pathogenesis. Recent clinical studies are targeting cytokines (IL-6 and IL-1) to modulate the innate immune response to prevent tissue damage and organ failure.
In this review paper, the authors highlight the benefits associated with modulating the immune response earlier in the process by inhibiting the migration of pro-inflammatory immune cells, interrupting the hyper-inflammation.
– Luiz Meirelles, DDS, MS, PhD
This abstract is available on the publisher's site.
An exacerbated and unbalanced immune response may account for the severity of COVID-19, the disease caused by the novel severe acute respiratory syndrome (SARS) coronavirus 2, SARS-CoV-2. In this Viewpoint, we summarize recent evidence for the role of neutrophils in the pathogenesis of COVID-19 and propose CXCR2 inhibition as a promising treatment option to block neutrophil recruitment and activation.